Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
Showing posts with label Kitava. Show all posts
Showing posts with label Kitava. Show all posts
Sunday, December 5, 2010
Interview with a Kitavan
Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
Interview with a Kitavan
Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
Interview with a Kitavan
Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.
How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.
Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.
Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.
What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.
Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.
Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.
How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.
Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.
Thanks for your help, Job! I know many people will appreciate reading these responses.
Wednesday, August 18, 2010
Tropical Plant Fats: Coconut Oil, Part I
Traditional Uses for Coconut
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Most palms begin to produce nuts about five years after germination and continue to yield them for forty to sixty years at a continuous (i.e., nonseasonal) rate, producing about fifty nuts a year. The immature nut contains a tangy liquid that in time transforms into a layer of hard, white flesh on the inner surface of the shell and, somewhat later, a spongy mass of embryo in the nut's cavity. The liquid of the immature nut was often drunk, and the spongy embryo of the mature nut often eaten, raw or cooked, but most nuts used for food were harvested after the meat had been deposited and before the embryo had begun to form...Mainstream Ire
After the nut had been split, the most common method of extracting its hardened flesh was by scraping it out of the shell with a saw-toothed tool of wood, shell, or stone, usually lashed to a three-footed stand. The shredded meat was then eaten either raw or mixed with some starchy food and then cooked, or had its oily cream extracted, by some form of squeezing, for cooking with other foods or for cosmetic or medical uses...
Those Polynesians fortunate enough to have coconut palms utilized their components not only for drink and food-- in some places the most important, indeed life-supporting food-- but also for building-frames, thatch, screens, caulking material, containers, matting, cordage, weapons, armor, cosmetics, medicine, etc.
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Tropical Plant Fats: Coconut Oil, Part I
Traditional Uses for Coconut
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Most palms begin to produce nuts about five years after germination and continue to yield them for forty to sixty years at a continuous (i.e., nonseasonal) rate, producing about fifty nuts a year. The immature nut contains a tangy liquid that in time transforms into a layer of hard, white flesh on the inner surface of the shell and, somewhat later, a spongy mass of embryo in the nut's cavity. The liquid of the immature nut was often drunk, and the spongy embryo of the mature nut often eaten, raw or cooked, but most nuts used for food were harvested after the meat had been deposited and before the embryo had begun to form...Mainstream Ire
After the nut had been split, the most common method of extracting its hardened flesh was by scraping it out of the shell with a saw-toothed tool of wood, shell, or stone, usually lashed to a three-footed stand. The shredded meat was then eaten either raw or mixed with some starchy food and then cooked, or had its oily cream extracted, by some form of squeezing, for cooking with other foods or for cosmetic or medical uses...
Those Polynesians fortunate enough to have coconut palms utilized their components not only for drink and food-- in some places the most important, indeed life-supporting food-- but also for building-frames, thatch, screens, caulking material, containers, matting, cordage, weapons, armor, cosmetics, medicine, etc.
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Tropical Plant Fats: Coconut Oil, Part I
Traditional Uses for Coconut
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Most palms begin to produce nuts about five years after germination and continue to yield them for forty to sixty years at a continuous (i.e., nonseasonal) rate, producing about fifty nuts a year. The immature nut contains a tangy liquid that in time transforms into a layer of hard, white flesh on the inner surface of the shell and, somewhat later, a spongy mass of embryo in the nut's cavity. The liquid of the immature nut was often drunk, and the spongy embryo of the mature nut often eaten, raw or cooked, but most nuts used for food were harvested after the meat had been deposited and before the embryo had begun to form...Mainstream Ire
After the nut had been split, the most common method of extracting its hardened flesh was by scraping it out of the shell with a saw-toothed tool of wood, shell, or stone, usually lashed to a three-footed stand. The shredded meat was then eaten either raw or mixed with some starchy food and then cooked, or had its oily cream extracted, by some form of squeezing, for cooking with other foods or for cosmetic or medical uses...
Those Polynesians fortunate enough to have coconut palms utilized their components not only for drink and food-- in some places the most important, indeed life-supporting food-- but also for building-frames, thatch, screens, caulking material, containers, matting, cordage, weapons, armor, cosmetics, medicine, etc.
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Tropical Plant Fats: Coconut Oil, Part I
Traditional Uses for Coconut
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Coconut palms are used for a variety of purposes throughout the tropics. Here are a few quotes from the book Polynesia in Early Historic Times:
Most palms begin to produce nuts about five years after germination and continue to yield them for forty to sixty years at a continuous (i.e., nonseasonal) rate, producing about fifty nuts a year. The immature nut contains a tangy liquid that in time transforms into a layer of hard, white flesh on the inner surface of the shell and, somewhat later, a spongy mass of embryo in the nut's cavity. The liquid of the immature nut was often drunk, and the spongy embryo of the mature nut often eaten, raw or cooked, but most nuts used for food were harvested after the meat had been deposited and before the embryo had begun to form...Mainstream Ire
After the nut had been split, the most common method of extracting its hardened flesh was by scraping it out of the shell with a saw-toothed tool of wood, shell, or stone, usually lashed to a three-footed stand. The shredded meat was then eaten either raw or mixed with some starchy food and then cooked, or had its oily cream extracted, by some form of squeezing, for cooking with other foods or for cosmetic or medical uses...
Those Polynesians fortunate enough to have coconut palms utilized their components not only for drink and food-- in some places the most important, indeed life-supporting food-- but also for building-frames, thatch, screens, caulking material, containers, matting, cordage, weapons, armor, cosmetics, medicine, etc.
Coconut fat is roughly 90 percent saturated, making it one of the most highly saturated fats on the planet. For this reason, it has been the subject of grave pronouncements by health authorities over the course of the last half century, resulting in its near elimination from the industrial food system. If the hypothesis that saturated fat causes heart disease and other health problems is correct, eating coconut oil regularly should tuck us in for a very long nap.
Coconut Eaters
As the Polynesians spread throughout the Eastern Pacific islands, they encountered shallow coral atolls that were not able to sustain their traditional starchy staples, taro, yams and breadfruit. Due to its extreme tolerance for poor, salty soils, the coconut palm was nearly the only food crop that would grow on these islands*. Therefore, their inhabitants lived almost exclusively on coconut and seafood for hundreds of years.
One group of islands that falls into this category is Tokelau, which fortunately for us was the subject of a major epidemiological study that spanned the years 1968 to 1982: the Tokelau Island Migrant Study (1). By this time, Tokelauans had managed to grow some starchy foods such as taro and breadfruit (introduced in the 20th century by Europeans), as well as obtaining some white flour and sugar, but their calories still came predominantly from coconut.
Over the time period in question, Tokelauans obtained roughly half their calories from coconut, placing them among the most extreme consumers of saturated fat in the world. Not only was their blood cholesterol lower than the average Westerner, but their hypertension rate was low, and physicians found no trace of previous heart attacks by ECG (age-adjusted rates: 0.0% in Tokelau vs 3.5% in Tecumseh USA). Migrating to New Zealand and cutting saturated fat intake in half was associated with a rise in ECG signs of heart attack (1.0% age-adjusted) (2, 3).
Diabetes was low in men and average in women by modern Western standards, but increased significantly upon migration to New Zealand and reduction of coconut intake (4). Non-migrant Tokelauans gained body fat at a slower rate than migrants, despite higher physical activity in the latter (5). Together, this evidence seriously challenges the idea that coconut is unhealthy.
The Kitavans also eat an amount of coconut fat that would make Dr. Ancel Keys blush. Dr. Staffan Lindeberg found that they got 21% of their 2,200 calories per day from fat, nearly all of which came from coconut. They were getting 17% of their calories from saturated fat; 55% more than the average American. Dr. Lindeberg's detailed series of studies found no trace of coronary heart disease or stroke, nor any obesity, diabetes or senile dementia even in the very old (6, 7).
Of course, the Tokelauans, Kitavans and other traditional cultures were not eating coconut in the form of refined, hydrogenated coconut oil cake icing. That distinction will be important when I discuss what the biomedical literature has to say in the next post.
* Most also had pandanus palms, which are also tolerant of poor soils and whose fruit provided a small amount of starch and sugar.
Tuesday, December 22, 2009
What's the Ideal Fasting Insulin Level?
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin prevents the escape of fat from fat tissue and causes a number of other metabolic disturbances.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
What's the Ideal Fasting Insulin Level?
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin prevents the escape of fat from fat tissue and causes a number of other metabolic disturbances.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
What's the Ideal Fasting Insulin Level?
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin prevents the escape of fat from fat tissue and causes a number of other metabolic disturbances.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
What's the Ideal Fasting Insulin Level?
Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin prevents the escape of fat from fat tissue and causes a number of other metabolic disturbances.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
Saturday, August 8, 2009
The Diet-Heart Hypothesis: Oxidized LDL, Part II
In the last post, I presented the evidence that oxidized LDL (oxLDL) is a dominant factor in the arterial disease known as atherosclerosis, although probably not the only factor. In this post, I'll describe some of the major contributors to oxLDL.
Polyunsaturated Fats Increase LDL Oxidation
The serum concentration of oxLDL is strongly influcenced by diet. One dietary determinant of oxLDL is dietary polyunsaturated fat (PUFA). PUFA are inherently susceptible to oxidative damage, compared to monounsaturated and saturated fats. The predominant PUFA in the modern diet is linoleic acid, found excessively in industrial seed oils like corn oil, sunflower oil, safflower oil, cottonseed oil and soy oil. LDL is naturally rich in linoleic acid, even in cultures such as the Kitavans who have a very low dietary intake of it. However, LDL content of linoleic acid does correlate with dietary intake, and the Kitavans have a comparatively small amount of linoleic acid in their LDL, relative to industrial cultures.
There have been a number of media reports in the last few years proclaiming that monounsaturated fat reduces LDL oxidation compared to saturated and polyunsaturated fat. This is rather implausible on the surface, so let's take a closer look. There are two ways to measure oxLDL:
Oops! LDL oxidation in the two PUFA groups was increased by more than 31%. The difference between the leftmost two groups and the rightmost two was statistically significant. As one would expect, oxidized LDL is proportional to the amount of PUFA in LDL, which is proportional to dietary PUFA. This somehow got left out of the abstract and media reports. The same investigators published a similar report a year later.
In another diet trial, participants were placed on one of two diets for 5 weeks: a low-fat, high PUFA diet low in vegetables; or a low-fat, high PUFA diet high in vegetables. The authors were forthright about their findings, so I'll let them summarize:
I suspect that the effect has less to do with the decrease in saturated fat and more to do with the increase in PUFA, although there's no way to know for sure. In the Lyon Diet-Heart trial, which I believe was the most successful diet trial of all time, linoleic acid was reduced to 3.6% of calories, but saturated fat was also reduced. Another reason is that there are numerous low-fat, low PUFA, high-carbohydrate cultures that have low levels of atherosclerosis and heart attacks. The Kitavans, for example, don't seem to have heart attacks or strokes (although no autopsies have been done so we don't know how much atherosclerosis they have).
They get 69% of their calories from high-glycemic starchy tubers, and their 21% fat comes mostly from coconut so it's highly saturated. Their blood lipids are low in omega-6 linoleic acid and very saturated. But there's a little surprise in the data: their lipids are full of palmitic acid (saturated), despite the fact that their diet contains very little of it. The reason is that their livers are turning all that carbohydrate into saturated fat, which is what happens when you eat more carbohydrate than you can burn immediately or store as glycogen. The moral of the story is that you don't need to eat saturated fat to have saturated LDL: a high-carbohydrate diet can accomplish the same thing, especially if it has a high glycemic index.
Fat-Soluble Antioxidants Decrease LDL Oxidation
LDL carries fat-soluble antioxidants, predominantly vitamin E and coenzyme Q10 (CoQ10). One form of vitamin E, alpha-tocopherol, slows atherosclerosis in most animal models but has shown equivocal results in human trials. There is even the suggestion that it may increase LDL oxidation under some circumstances. I don't recommend supplementing with vitamin E. However, the first line of antioxidant defense in LDL is provided by CoQ10. CoQ10 unequivocally reduces LDL oxidation in human subjects, and potently reduces atherosclerosis in animal models.
CoQ10 has a special relationship with cardiovascular health. Levels are reduced in individuals with cardiovascular disease and high oxLDL. Whether this is cause or effect, it's difficult to say. However, supplementing with CoQ10 has been repeatedly shown to be effective for high blood pressure and congestive heart failure. There has been one controlled trial of CoQ10 (120 mg/day) supplementation for the prevention of heart attacks, which reduced cardiac events including deaths by 45%, compared to a group receiving B vitamins. The CoQ10 group showed a large reduction in plasma lipid oxidation. This is a promising result and the experiment should be repeated.
CoQ10 is not an essential nutrient, although food does contribute a small portion of our total CoQ10 use. The large majority of CoQ10 is synthesized by the body itself, and this is dependent on a number of essential nutrients, including vitamin B2, B3, B5, B6, B12, vitamin C and folic acid. Thus, the body's synthesis of CoQ10 is dependent on overall nutritional status. Sub-clinical deficiency of any of these vitamins can hypothetically contribute to reduced CoQ10 production and thus oxLDL. This is potentially a big problem since modern Americans get more than half their calories from nutrient-poor refined foods. Liver is the single best source of many of these vitamins, and also holds the title of Most Nutritious Food on the Planet. It's also rich in CoQ10.
CoQ10 synthesis declines with age and is reduced in people with disorders involving oxidative stress, like cardiovascular disease. It's also greatly reduced by the cholesterol-lowering drugs statins. I'm not generally in favor of supplements, but CoQ10 seems to have a lot of promise and nothing but positive side effects that I'm aware of. CoQ10 deficiency may be a common theme in a number of modern disorders.
Excess Blood Sugar and Fructose Increase LDL Oxidation
Both type I and type II diabetes are associated with higher levels of oxLDL, therefore, prolonged high blood glucose may contribute to LDL oxidation due to glycosylation of the LDL protein ApoB. Fructose consumption increases oxLDL relative to glucose. Fructose is a very powerful glycosylating agent (binds non-specifically to other molecules, causing damage). Although it isn't present at high levels in the general circulation, it does interact with blood lipids in the hepatic portal vein as it moves from the digestive tract to the liver to be turned into fat (palmitic acid). Peter at Hyperlipid has written extensively about the role of glycosylation in LDL oxidation.
The Diet-Heart Hypothesis: The Verdict
The diet-heart hypothesis, the idea that dietary saturated fat and cholesterol raise blood cholesterol and thus increase heart attack risk, is a half-century embarrassment to the international scientific community. It requires willful ignorance of the fact that saturated fat does not increase total cholesterol or LDL in humans, in the long term. It requires a simplistic view of blood lipids that ignores the potentially harmful effects of replacing animal fats with carbohydrate or industrial seed oils. Worst of all, it requires selective citation of the literature on diet modification trials.
I have to conclude that if dietary saturated fat and cholesterol play any role whatsoever in cardiovascular disease, it's a minor one that's trumped by other factors. Industrial seed oils and sugar are likely to play an important role in cardiovascular disease.
Polyunsaturated Fats Increase LDL Oxidation
The serum concentration of oxLDL is strongly influcenced by diet. One dietary determinant of oxLDL is dietary polyunsaturated fat (PUFA). PUFA are inherently susceptible to oxidative damage, compared to monounsaturated and saturated fats. The predominant PUFA in the modern diet is linoleic acid, found excessively in industrial seed oils like corn oil, sunflower oil, safflower oil, cottonseed oil and soy oil. LDL is naturally rich in linoleic acid, even in cultures such as the Kitavans who have a very low dietary intake of it. However, LDL content of linoleic acid does correlate with dietary intake, and the Kitavans have a comparatively small amount of linoleic acid in their LDL, relative to industrial cultures.
There have been a number of media reports in the last few years proclaiming that monounsaturated fat reduces LDL oxidation compared to saturated and polyunsaturated fat. This is rather implausible on the surface, so let's take a closer look. There are two ways to measure oxLDL:
- Measure it directly from the blood
- Take normal LDL from the blood, expose it to copper in a test tube, and see how fast it oxidizes
LDL resistance to copper-induced oxidation, expressed as lag time, was highest during the MUFA-rich diet (55.1±7.3 minutes) and lowest during the PUFA(n-3)– (45.3±7 minutes) and SFA- (45.3±6.4 minutes) rich diets.This was published in a paper by P. Mata and colleagues in 1996. They fed 42 volunteers one of four different diets for 5 weeks each: one rich in saturated fat, one rich in monounsaturated fat, one rich in linoleic acid PUFA, and one rich in linoleic acid plus omega-3 PUFA. They emphasized the finding quoted above, as did the media. But there's an embarrassing piece of data buried in the paper that the authors, and the media, ignored (thanks to Chris Masterjohn for pointing this out). Here's what they saw when they looked directly at LDL oxidation in their volunteers:
Oops! LDL oxidation in the two PUFA groups was increased by more than 31%. The difference between the leftmost two groups and the rightmost two was statistically significant. As one would expect, oxidized LDL is proportional to the amount of PUFA in LDL, which is proportional to dietary PUFA. This somehow got left out of the abstract and media reports. The same investigators published a similar report a year later.In another diet trial, participants were placed on one of two diets for 5 weeks: a low-fat, high PUFA diet low in vegetables; or a low-fat, high PUFA diet high in vegetables. The authors were forthright about their findings, so I'll let them summarize:
The median plasma OxLDL-EO6 increased by 27% (P less than 0.01) in response to the low-fat, low-vegetable diet and 19% (P less than 0.01) in response to the low-fat, high-vegetable diet. Also, the Lp(a) concentration was increased by 7% (P less than 0.01) and 9% (P=0.01), respectively.This is the diet mainstream cardiologists have been prescribing to heart attack patients for 40 years. The trials I mentioned above are the only three I'm aware of in which fat quality was manipulated and oxLDL was directly measured (the first two were based on subsets of the same data). They all suggest that replacing saturated fat with PUFA increases oxLDL.
I suspect that the effect has less to do with the decrease in saturated fat and more to do with the increase in PUFA, although there's no way to know for sure. In the Lyon Diet-Heart trial, which I believe was the most successful diet trial of all time, linoleic acid was reduced to 3.6% of calories, but saturated fat was also reduced. Another reason is that there are numerous low-fat, low PUFA, high-carbohydrate cultures that have low levels of atherosclerosis and heart attacks. The Kitavans, for example, don't seem to have heart attacks or strokes (although no autopsies have been done so we don't know how much atherosclerosis they have).
They get 69% of their calories from high-glycemic starchy tubers, and their 21% fat comes mostly from coconut so it's highly saturated. Their blood lipids are low in omega-6 linoleic acid and very saturated. But there's a little surprise in the data: their lipids are full of palmitic acid (saturated), despite the fact that their diet contains very little of it. The reason is that their livers are turning all that carbohydrate into saturated fat, which is what happens when you eat more carbohydrate than you can burn immediately or store as glycogen. The moral of the story is that you don't need to eat saturated fat to have saturated LDL: a high-carbohydrate diet can accomplish the same thing, especially if it has a high glycemic index.
Fat-Soluble Antioxidants Decrease LDL Oxidation
LDL carries fat-soluble antioxidants, predominantly vitamin E and coenzyme Q10 (CoQ10). One form of vitamin E, alpha-tocopherol, slows atherosclerosis in most animal models but has shown equivocal results in human trials. There is even the suggestion that it may increase LDL oxidation under some circumstances. I don't recommend supplementing with vitamin E. However, the first line of antioxidant defense in LDL is provided by CoQ10. CoQ10 unequivocally reduces LDL oxidation in human subjects, and potently reduces atherosclerosis in animal models.
CoQ10 has a special relationship with cardiovascular health. Levels are reduced in individuals with cardiovascular disease and high oxLDL. Whether this is cause or effect, it's difficult to say. However, supplementing with CoQ10 has been repeatedly shown to be effective for high blood pressure and congestive heart failure. There has been one controlled trial of CoQ10 (120 mg/day) supplementation for the prevention of heart attacks, which reduced cardiac events including deaths by 45%, compared to a group receiving B vitamins. The CoQ10 group showed a large reduction in plasma lipid oxidation. This is a promising result and the experiment should be repeated.
CoQ10 is not an essential nutrient, although food does contribute a small portion of our total CoQ10 use. The large majority of CoQ10 is synthesized by the body itself, and this is dependent on a number of essential nutrients, including vitamin B2, B3, B5, B6, B12, vitamin C and folic acid. Thus, the body's synthesis of CoQ10 is dependent on overall nutritional status. Sub-clinical deficiency of any of these vitamins can hypothetically contribute to reduced CoQ10 production and thus oxLDL. This is potentially a big problem since modern Americans get more than half their calories from nutrient-poor refined foods. Liver is the single best source of many of these vitamins, and also holds the title of Most Nutritious Food on the Planet. It's also rich in CoQ10.
CoQ10 synthesis declines with age and is reduced in people with disorders involving oxidative stress, like cardiovascular disease. It's also greatly reduced by the cholesterol-lowering drugs statins. I'm not generally in favor of supplements, but CoQ10 seems to have a lot of promise and nothing but positive side effects that I'm aware of. CoQ10 deficiency may be a common theme in a number of modern disorders.
Excess Blood Sugar and Fructose Increase LDL Oxidation
Both type I and type II diabetes are associated with higher levels of oxLDL, therefore, prolonged high blood glucose may contribute to LDL oxidation due to glycosylation of the LDL protein ApoB. Fructose consumption increases oxLDL relative to glucose. Fructose is a very powerful glycosylating agent (binds non-specifically to other molecules, causing damage). Although it isn't present at high levels in the general circulation, it does interact with blood lipids in the hepatic portal vein as it moves from the digestive tract to the liver to be turned into fat (palmitic acid). Peter at Hyperlipid has written extensively about the role of glycosylation in LDL oxidation.
The Diet-Heart Hypothesis: The Verdict
The diet-heart hypothesis, the idea that dietary saturated fat and cholesterol raise blood cholesterol and thus increase heart attack risk, is a half-century embarrassment to the international scientific community. It requires willful ignorance of the fact that saturated fat does not increase total cholesterol or LDL in humans, in the long term. It requires a simplistic view of blood lipids that ignores the potentially harmful effects of replacing animal fats with carbohydrate or industrial seed oils. Worst of all, it requires selective citation of the literature on diet modification trials.
I have to conclude that if dietary saturated fat and cholesterol play any role whatsoever in cardiovascular disease, it's a minor one that's trumped by other factors. Industrial seed oils and sugar are likely to play an important role in cardiovascular disease.
The Diet-Heart Hypothesis: Oxidized LDL, Part II
In the last post, I presented the evidence that oxidized LDL (oxLDL) is a dominant factor in the arterial disease known as atherosclerosis, although probably not the only factor. In this post, I'll describe some of the major contributors to oxLDL.
Polyunsaturated Fats Increase LDL Oxidation
The serum concentration of oxLDL is strongly influcenced by diet. One dietary determinant of oxLDL is dietary polyunsaturated fat (PUFA). PUFA are inherently susceptible to oxidative damage, compared to monounsaturated and saturated fats. The predominant PUFA in the modern diet is linoleic acid, found excessively in industrial seed oils like corn oil, sunflower oil, safflower oil, cottonseed oil and soy oil. LDL is naturally rich in linoleic acid, even in cultures such as the Kitavans who have a very low dietary intake of it. However, LDL content of linoleic acid does correlate with dietary intake, and the Kitavans have a comparatively small amount of linoleic acid in their LDL, relative to industrial cultures.
There have been a number of media reports in the last few years proclaiming that monounsaturated fat reduces LDL oxidation compared to saturated and polyunsaturated fat. This is rather implausible on the surface, so let's take a closer look. There are two ways to measure oxLDL:
Oops! LDL oxidation in the two PUFA groups was increased by more than 31%. The difference between the leftmost two groups and the rightmost two was statistically significant. As one would expect, oxidized LDL is proportional to the amount of PUFA in LDL, which is proportional to dietary PUFA. This somehow got left out of the abstract and media reports. The same investigators published a similar report a year later.
In another diet trial, participants were placed on one of two diets for 5 weeks: a low-fat, high PUFA diet low in vegetables; or a low-fat, high PUFA diet high in vegetables. The authors were forthright about their findings, so I'll let them summarize:
I suspect that the effect has less to do with the decrease in saturated fat and more to do with the increase in PUFA, although there's no way to know for sure. In the Lyon Diet-Heart trial, which I believe was the most successful diet trial of all time, linoleic acid was reduced to 3.6% of calories, but saturated fat was also reduced. Another reason is that there are numerous low-fat, low PUFA, high-carbohydrate cultures that have low levels of atherosclerosis and heart attacks. The Kitavans, for example, don't seem to have heart attacks or strokes (although no autopsies have been done so we don't know how much atherosclerosis they have).
They get 69% of their calories from high-glycemic starchy tubers, and their 21% fat comes mostly from coconut so it's highly saturated. Their blood lipids are low in omega-6 linoleic acid and very saturated. But there's a little surprise in the data: their lipids are full of palmitic acid (saturated), despite the fact that their diet contains very little of it. The reason is that their livers are turning all that carbohydrate into saturated fat, which is what happens when you eat more carbohydrate than you can burn immediately or store as glycogen. The moral of the story is that you don't need to eat saturated fat to have saturated LDL: a high-carbohydrate diet can accomplish the same thing, especially if it has a high glycemic index.
Fat-Soluble Antioxidants Decrease LDL Oxidation
LDL carries fat-soluble antioxidants, predominantly vitamin E and coenzyme Q10 (CoQ10). One form of vitamin E, alpha-tocopherol, slows atherosclerosis in most animal models but has shown equivocal results in human trials. There is even the suggestion that it may increase LDL oxidation under some circumstances. I don't recommend supplementing with vitamin E. However, the first line of antioxidant defense in LDL is provided by CoQ10. CoQ10 unequivocally reduces LDL oxidation in human subjects, and potently reduces atherosclerosis in animal models.
CoQ10 has a special relationship with cardiovascular health. Levels are reduced in individuals with cardiovascular disease and high oxLDL. Whether this is cause or effect, it's difficult to say. However, supplementing with CoQ10 has been repeatedly shown to be effective for high blood pressure and congestive heart failure. There has been one controlled trial of CoQ10 (120 mg/day) supplementation for the prevention of heart attacks, which reduced cardiac events including deaths by 45%, compared to a group receiving B vitamins. The CoQ10 group showed a large reduction in plasma lipid oxidation. This is a promising result and the experiment should be repeated.
CoQ10 is not an essential nutrient, although food does contribute a small portion of our total CoQ10 use. The large majority of CoQ10 is synthesized by the body itself, and this is dependent on a number of essential nutrients, including vitamin B2, B3, B5, B6, B12, vitamin C and folic acid. Thus, the body's synthesis of CoQ10 is dependent on overall nutritional status. Sub-clinical deficiency of any of these vitamins can hypothetically contribute to reduced CoQ10 production and thus oxLDL. This is potentially a big problem since modern Americans get more than half their calories from nutrient-poor refined foods. Liver is the single best source of many of these vitamins, and also holds the title of Most Nutritious Food on the Planet. It's also rich in CoQ10.
CoQ10 synthesis declines with age and is reduced in people with disorders involving oxidative stress, like cardiovascular disease. It's also greatly reduced by the cholesterol-lowering drugs statins. I'm not generally in favor of supplements, but CoQ10 seems to have a lot of promise and nothing but positive side effects that I'm aware of. CoQ10 deficiency may be a common theme in a number of modern disorders.
Excess Blood Sugar and Fructose Increase LDL Oxidation
Both type I and type II diabetes are associated with higher levels of oxLDL, therefore, prolonged high blood glucose may contribute to LDL oxidation due to glycosylation of the LDL protein ApoB. Fructose consumption increases oxLDL relative to glucose. Fructose is a very powerful glycosylating agent (binds non-specifically to other molecules, causing damage). Although it isn't present at high levels in the general circulation, it does interact with blood lipids in the hepatic portal vein as it moves from the digestive tract to the liver to be turned into fat (palmitic acid). Peter at Hyperlipid has written extensively about the role of glycosylation in LDL oxidation.
The Diet-Heart Hypothesis: The Verdict
The diet-heart hypothesis, the idea that dietary saturated fat and cholesterol raise blood cholesterol and thus increase heart attack risk, is a half-century embarrassment to the international scientific community. It requires willful ignorance of the fact that saturated fat does not increase total cholesterol or LDL in humans, in the long term. It requires a simplistic view of blood lipids that ignores the potentially harmful effects of replacing animal fats with carbohydrate or industrial seed oils. Worst of all, it requires selective citation of the literature on diet modification trials.
I have to conclude that if dietary saturated fat and cholesterol play any role whatsoever in cardiovascular disease, it's a minor one that's trumped by other factors. Industrial seed oils and sugar are likely to play an important role in cardiovascular disease.
Polyunsaturated Fats Increase LDL Oxidation
The serum concentration of oxLDL is strongly influcenced by diet. One dietary determinant of oxLDL is dietary polyunsaturated fat (PUFA). PUFA are inherently susceptible to oxidative damage, compared to monounsaturated and saturated fats. The predominant PUFA in the modern diet is linoleic acid, found excessively in industrial seed oils like corn oil, sunflower oil, safflower oil, cottonseed oil and soy oil. LDL is naturally rich in linoleic acid, even in cultures such as the Kitavans who have a very low dietary intake of it. However, LDL content of linoleic acid does correlate with dietary intake, and the Kitavans have a comparatively small amount of linoleic acid in their LDL, relative to industrial cultures.
There have been a number of media reports in the last few years proclaiming that monounsaturated fat reduces LDL oxidation compared to saturated and polyunsaturated fat. This is rather implausible on the surface, so let's take a closer look. There are two ways to measure oxLDL:
- Measure it directly from the blood
- Take normal LDL from the blood, expose it to copper in a test tube, and see how fast it oxidizes
LDL resistance to copper-induced oxidation, expressed as lag time, was highest during the MUFA-rich diet (55.1±7.3 minutes) and lowest during the PUFA(n-3)– (45.3±7 minutes) and SFA- (45.3±6.4 minutes) rich diets.This was published in a paper by P. Mata and colleagues in 1996. They fed 42 volunteers one of four different diets for 5 weeks each: one rich in saturated fat, one rich in monounsaturated fat, one rich in linoleic acid PUFA, and one rich in linoleic acid plus omega-3 PUFA. They emphasized the finding quoted above, as did the media. But there's an embarrassing piece of data buried in the paper that the authors, and the media, ignored (thanks to Chris Masterjohn for pointing this out). Here's what they saw when they looked directly at LDL oxidation in their volunteers:
Oops! LDL oxidation in the two PUFA groups was increased by more than 31%. The difference between the leftmost two groups and the rightmost two was statistically significant. As one would expect, oxidized LDL is proportional to the amount of PUFA in LDL, which is proportional to dietary PUFA. This somehow got left out of the abstract and media reports. The same investigators published a similar report a year later.In another diet trial, participants were placed on one of two diets for 5 weeks: a low-fat, high PUFA diet low in vegetables; or a low-fat, high PUFA diet high in vegetables. The authors were forthright about their findings, so I'll let them summarize:
The median plasma OxLDL-EO6 increased by 27% (P less than 0.01) in response to the low-fat, low-vegetable diet and 19% (P less than 0.01) in response to the low-fat, high-vegetable diet. Also, the Lp(a) concentration was increased by 7% (P less than 0.01) and 9% (P=0.01), respectively.This is the diet mainstream cardiologists have been prescribing to heart attack patients for 40 years. The trials I mentioned above are the only three I'm aware of in which fat quality was manipulated and oxLDL was directly measured (the first two were based on subsets of the same data). They all suggest that replacing saturated fat with PUFA increases oxLDL.
I suspect that the effect has less to do with the decrease in saturated fat and more to do with the increase in PUFA, although there's no way to know for sure. In the Lyon Diet-Heart trial, which I believe was the most successful diet trial of all time, linoleic acid was reduced to 3.6% of calories, but saturated fat was also reduced. Another reason is that there are numerous low-fat, low PUFA, high-carbohydrate cultures that have low levels of atherosclerosis and heart attacks. The Kitavans, for example, don't seem to have heart attacks or strokes (although no autopsies have been done so we don't know how much atherosclerosis they have).
They get 69% of their calories from high-glycemic starchy tubers, and their 21% fat comes mostly from coconut so it's highly saturated. Their blood lipids are low in omega-6 linoleic acid and very saturated. But there's a little surprise in the data: their lipids are full of palmitic acid (saturated), despite the fact that their diet contains very little of it. The reason is that their livers are turning all that carbohydrate into saturated fat, which is what happens when you eat more carbohydrate than you can burn immediately or store as glycogen. The moral of the story is that you don't need to eat saturated fat to have saturated LDL: a high-carbohydrate diet can accomplish the same thing, especially if it has a high glycemic index.
Fat-Soluble Antioxidants Decrease LDL Oxidation
LDL carries fat-soluble antioxidants, predominantly vitamin E and coenzyme Q10 (CoQ10). One form of vitamin E, alpha-tocopherol, slows atherosclerosis in most animal models but has shown equivocal results in human trials. There is even the suggestion that it may increase LDL oxidation under some circumstances. I don't recommend supplementing with vitamin E. However, the first line of antioxidant defense in LDL is provided by CoQ10. CoQ10 unequivocally reduces LDL oxidation in human subjects, and potently reduces atherosclerosis in animal models.
CoQ10 has a special relationship with cardiovascular health. Levels are reduced in individuals with cardiovascular disease and high oxLDL. Whether this is cause or effect, it's difficult to say. However, supplementing with CoQ10 has been repeatedly shown to be effective for high blood pressure and congestive heart failure. There has been one controlled trial of CoQ10 (120 mg/day) supplementation for the prevention of heart attacks, which reduced cardiac events including deaths by 45%, compared to a group receiving B vitamins. The CoQ10 group showed a large reduction in plasma lipid oxidation. This is a promising result and the experiment should be repeated.
CoQ10 is not an essential nutrient, although food does contribute a small portion of our total CoQ10 use. The large majority of CoQ10 is synthesized by the body itself, and this is dependent on a number of essential nutrients, including vitamin B2, B3, B5, B6, B12, vitamin C and folic acid. Thus, the body's synthesis of CoQ10 is dependent on overall nutritional status. Sub-clinical deficiency of any of these vitamins can hypothetically contribute to reduced CoQ10 production and thus oxLDL. This is potentially a big problem since modern Americans get more than half their calories from nutrient-poor refined foods. Liver is the single best source of many of these vitamins, and also holds the title of Most Nutritious Food on the Planet. It's also rich in CoQ10.
CoQ10 synthesis declines with age and is reduced in people with disorders involving oxidative stress, like cardiovascular disease. It's also greatly reduced by the cholesterol-lowering drugs statins. I'm not generally in favor of supplements, but CoQ10 seems to have a lot of promise and nothing but positive side effects that I'm aware of. CoQ10 deficiency may be a common theme in a number of modern disorders.
Excess Blood Sugar and Fructose Increase LDL Oxidation
Both type I and type II diabetes are associated with higher levels of oxLDL, therefore, prolonged high blood glucose may contribute to LDL oxidation due to glycosylation of the LDL protein ApoB. Fructose consumption increases oxLDL relative to glucose. Fructose is a very powerful glycosylating agent (binds non-specifically to other molecules, causing damage). Although it isn't present at high levels in the general circulation, it does interact with blood lipids in the hepatic portal vein as it moves from the digestive tract to the liver to be turned into fat (palmitic acid). Peter at Hyperlipid has written extensively about the role of glycosylation in LDL oxidation.
The Diet-Heart Hypothesis: The Verdict
The diet-heart hypothesis, the idea that dietary saturated fat and cholesterol raise blood cholesterol and thus increase heart attack risk, is a half-century embarrassment to the international scientific community. It requires willful ignorance of the fact that saturated fat does not increase total cholesterol or LDL in humans, in the long term. It requires a simplistic view of blood lipids that ignores the potentially harmful effects of replacing animal fats with carbohydrate or industrial seed oils. Worst of all, it requires selective citation of the literature on diet modification trials.
I have to conclude that if dietary saturated fat and cholesterol play any role whatsoever in cardiovascular disease, it's a minor one that's trumped by other factors. Industrial seed oils and sugar are likely to play an important role in cardiovascular disease.
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